Intergrative Session: Dive and Climb Flashcards
What mechanisms increase the diffusing capacity of the lungs with acclimatization to high altitude
Fick’s Law: want to ↑SA, ↑P1-P2 (by ↑P1 and/or ↓P2)
↑VE (more alveoli ventilated) ↑SA
Open and dilate pulmonary capillaries = ↑SA , ↑pulmonary artery pressure (but would ↑T if ↑PAP promotes oedema)
↑blood volume ↑SA
↑HCT & ↑[Hb] ↑blood O2 carry capacity, helps ↑P1-P2 by ↓P2
Pulmonary angiogenesis ↑SA
Climber Kent has just arrived at Mt Everest base camp after the 3 day trek from the nearest village. What acid-base disturbance would he mostly be experiencing on his initial rapid ascent to high altitude and explain why?
Respiratory Alkalosis
↓PB ↓PiO2 ↓PAO2 ↓PaO2 stimulates hyperventilation (↑ VE relative to VO2) ↓PaCO2 which ↓arterial H+
B = barometric i = inspired A = Alveolar a = arterial
MOVES THE EQUATION LEFT:
CO2 + H2O <–> H2CO3<–> H+ + HCO3
What compensation mechanism would be employed in response to the altitude induced acid base disturbance?
Renal retention of H+, and↑secretion of HCO3
↑removal of HCO3-leads to diuresis & dehydration unless adequate ↑ fluid intake
A headache at altitude isn’t always altitiude sickness/high altitude cerebral edema, dehydration also likely.
Headache at altitude without significant altitude gain (<500m/day) and no other AMS symptoms: drink 1L H2O (or electrolytes), take ibuprofen, wait 30 mins and reassess, i.e. correct dehydration
Acetazolamide (Diamox) can used to prevent & reduce the symptoms of altitude sicknesswhen rapid ascent is unavoidable. What is its mechanism of action and how would it help to reduce the symptoms of altitude sickness?
Acetazolamide (Diamox): inhibits carbonic anhydrase, ↓reabsorption of HCO3- in PCT thus facilitates renal loss of HCO3-. By ↓respiratory alkalosis induced by hypocapnia, it helps to facilitate ↑ ventilation by mitigating hypocapnic loss of central respiratory drive
Describe the breathing pattern commonly detected during sleep at high altitude and describe the mechanism(s) that underpins this breathing pattern
Cheyne-Stokes Respiration (describe pattern - its in picture)
High altitude:
Hypoxia causes hypoxemia (low blood O2) •
Stimulates VRG & DRG via peripheral chemoreceptors (weak but fast) to ↑VE •
Hyperventilation PaO2 and PaCO2 (pH) •
PaCO2 (pH) ↓VE via central chemoreceptors via RTN neurons (slow but strong) •
Problem exists because there are 2 competing signals (hypoxic stimulation and simultaneous hypocapnic depression) and there is ↑ lag time between changes in lung gases and central chemoreceptor response
Describe the feedback loop involved in the cough reflex
Reflex mechanism • rids the respiratory tract of any irritant that enters through the air and less frequently any fluids (drinks) and solids (food) • Can be initiated voluntarily but lacks the force and pressure as when triggered by the cough reflex
Cough receptors: rapidly adapting receptors at pharynx, trachea (carina), bronchi and bronchioles •
Afferent nerves: vagus and glossopharyngeal •
Control Centre: cough centre in medulla •
Efferent nerves: vagus, phrenic and spinal motor •
Effector muscles: glottis, external intercostals, diaphragm, major inspiratory and expiratory muscles
Describe the sequence of events involve in a cough
Inspiratory phase: Deep and sudden inhalation fills the lungs with up to 2.5 liters of air
Compression phase: The epiglottis closes and the vocal cords contract to close the larynx fully The abdominal muscles contract with force and push against the diaphragm Simultaneous forceful contraction of accessory muscles of expiration ↑ pulmonary pressure
Expiratory Phase: When pressure is sufficiently high, the vocal cords relax and the epiglottis suddenly opens ↑pulmonary pressure rushes out almost in an explosive manner The pressure also causes the bronchi and parts of the trachea to narrow to form slits through which the high airflow rate can sweep out any irritants
How can the trachea act to increase the velocity of expiratory air during a cough?
• Contraction of the trachealis muscle ↓ trachea diameter •
↑ air velocity further and aids mucus (obstruction) clearance
Climber Kent returns to Everest base camp after successfully summiting Everest for the 2nd time in a week. He has lost a considerable amount of weight, has a weak, hoarse voice and complains of fatigue and a very sore throat. On examination at HRA clinic at base camp he was found to have a persistent dry cough, Hbsat 77%, absent breath sounds and no peripheral cyanosis.
Are Kent’s symptoms consistent with a presentation of HAPE?
What is the diagnosis?
If cough is dry and %Hbsat is normal (for that altitude) then HAPE unlikely HAPE - %Hbsat for altitude, productive cough, abnormal breath sounds, peripheral cyanosis)
Khumbu cough
If Kent was suffering from HAPE, explain step by step the development of this condition and the resulting decrease in gas exchange efficiency?
HAPE = High altitude pulmonary edema
High altitude = ↓barometric pressure (PB) = PiO2 PAO2
↓PAO2 diffusion ax respiratory membrane = PaO2 (A-a diff = normal)
Induces pulmonary hypoxic vasoconstriction, which pulmonary arterial pressure (PAP)
PAP hydrostatic pressure in pulmonary artery beyond the capacity for fluid reabsorption by venous and lymphatic systems •Fluid build up in the lungs = pulmonary oedema •Oedema thickness of the respiratory membrane and further the efficiency of gas exchange
CURE: descend to lower altitudes
David (unfit dad) and young son go diving. At 150 feet jack notices david is acting weird.
What is the likely cause (and mechanism) of David’s odd behaviour?
How should Jack respond to this situation? If he did not respond, what issues may have arisen?
Both David and his son are diving at the same depth breathing the same air mixture, why might David be more likely to be at risk of DCS?
– Nitrogen Narcosis – N2 at ↑P dissolves in cell membranes. Alters the ionic conductance of neuron membranes and ↓ neuronal excitability
– Ascend immediately (with decompression stops if required and safe to do so) – If not, run out of air and may have make a rapid ascent – Nitrogen Narcosis could worsen if doesn’t ascend
–Nitrogen ~5x more soluble in fat –Not likely to affect level of nitrogen narcosis
How does hyperbaric treatment help with the problems associated with decompression illness?
High pressure will compress the N2 bubbles (↑Pressure ↓volume - link to Boyles Law) and prevent them from blocking vessels. Pressure can then be reduced slowly, allowing N2 to be removed slowly without large bubble formation.
Girl is running low on air at the end of dive and cuts her safety decompression stops short. On surfacing, Fatimah is in severe discomfort, is unable to stand properly. She has sub sternum pain worsening with deep inspirations, dyspnoea and cough. She collapses and becomes comatose. After appropriate treatment, she feels fine.
What is the likely explanation for Fatimah’s condition?
What treatment is Fatimah likely to have been given?
- –Decompression Sickness
- Arterial gas embolism
- Chokes
- CAGE (cerebral artery gas embolism)
– Immediate Oxygen (100% preferred) – Decompression Chamber (Hyperbaric Therapy)
Which organs/structures in the body are going to be susceptible to the barotrauma associated with diving?
Any gas filled spaces/organs, including the lungs, middle/inner ears, sinuses, nasal passages and the interior of hollow organs (stomach and intestines) Pulmonary barotrauma (pulmonary over pressurization syndrome, POPS, or burst lung) can occur if the diver fails to expel air from the lungs during ascent. As the diver ascends, ↓P = ↑ volume of gas in the lung
What are some contraindications for SCUBA diving?
And why are these contraindicated?
- Lung conditions
- Asthma
- Lung cysts
- Previous spontaneous pneumothorax
- Obstructive lung disease
- Lungs which empty unevenly (X-ray appearance)
- Previous thoracotomy
Any condition that impedes expiration/lung emptying and/or increases risk of lung rupture Obstructive conditions – prolonged time for expiration due to increased airway resistance and dynamic airway collapse on expiration
why can you not fly after you dive
